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Stage 2 Cheat sheets > BP > Flashcards

BP Flashcards

1
Q

3 anti fungal drugs and their targets

A

Azoles - block alpha 14 demethylase (a fungal cytochrome P450) = formation of ergosterol = increased cell wall permeability, inhibition of replication
Polyenes - bind to sterols in the membrane, bind to ergosterol with higher affinity - forms ion channel = loss of rigidity
Mitotic inhibitors = inhibit cell division by interfering with spindle formation

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2
Q

3 main administration methods for anti-fungals

A

Oral
IV
Topical

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3
Q

Calculate clearance

A

Cl = Vd x Ke

Dose/AUC

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4
Q

Ke

A

Elimination constant

0.693/half life

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5
Q

Vd

A

Volume of distribution

Drug in body/drug in plasma conc

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6
Q

Why is clauvanic acid commonly prescribed with beat lactic antibiotics?

A

Inhibits beta lactamases which break down beta lactic antibiotics

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7
Q

Graded Vs Quantal curves

A

Graded looks at the response of an individual with increased concentration
Quantal looks at a specific response of a population with an increased concentration
Graded = sigmoidal
Quantal = n

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8
Q

What 2 drugs increase likelihood of candidiasis infection?

A

Glucocorticosteroids

Immunosuppressants

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9
Q

What type of drug is morphine?

What is it used to treat?

A

Opioid

Moderate to severe pain, terminal care

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10
Q

What type of drug is codeine?
What is it used to treat?
Side effects?

A

Weak opioid
Mild to moderate pain, cough suppression, antidiarrhoeal
Constipation

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11
Q

Where do benzodiazepine accumulate, why?
Side effects
Mechanism of action

A

Body fat because they have a high lipid solubility
Long lasting hangover, amnesia, sexual fantasies, dependency
Binds to specific regulatory site on the GABAa receptor - increasing the affinity for GABAa molecule = increased frequency of binding = increased inhibition of neuronal signals to brain = treat anxiety

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12
Q

How do benzodiazepines differ from barbiturates?

A

Barbituates increase the binding duration of GABA, benzodiazepines increase the frequency of binding

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13
Q

2 ways of sedating a patient other than benzodiazepine?

A

Inhalation of nitric acid

H1 antagonist

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14
Q

What does heparin bind to? mechanism of action?

What is a better version of heparin, why?

A

Antithrombin
Binds to antithrombin III which accelerates the inhibition of thrombin and clotting factors
Low molecular weight heparins have more constant activity because they only bind antithrombin III

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15
Q

How is heparin administered? why?

A

IV or SC

Not absorbed from the gut (high PPB)

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16
Q

Method of warfarin administration?

A

Oral

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17
Q

Mechanism of action of warfarin?

A

Inhibits hepatic synthesis of vit K dependent clothing factors by inhibiting vit K reductase

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18
Q

Speed of action for warfarin?

A

1-2 days

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19
Q

What does aspirin cause?

A

NSAID = anti platelet, antipyretic, analgesic, anti-inflammtory

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20
Q

How does aspirin have an antiplatelet action?

A

Inhibits eiconsaoid production by inhibiting COX
Inhibits COX mediated release of TXA2 and PGI2
TXA2 = promotes aggregation
PGI2 = inhibits aggregation
PGI2 is endothelium derived so makes more
TGA2 is platelet derived so no more made
= reduce platelet aggregation

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21
Q

How do antidepressants work?

A

TCA’s inhibit 5-HT and NA reuptake but this isn’t selective to also blocks M1 H1 and alpha 1
SSRI are selective
Monamine oxidase inhibitors = block the breakdown of Na to amines
More NA or 5HT in neurotransmitter in synapse

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22
Q

How do antidepressants cause dry mouth?

A

TCA are not selective block M1 receptors = block parasympathetic effects = decreased saliva flow = dry mouth

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23
Q

Mechanism of action of LA?

A

Block electrical signalling in neurones by blocking Na+ channels

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24
Q

How to calculate half life?

A

From graph or 0.693/Ke

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25
Q

2 pregnancy hormones related from anterior pituitary gland and function of each?

A 
FSH = development of follicle
LH = caused progesterone release from ovaries
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26
Q

2 pregnancy hormones related from ovary? function?

A

Progesterone - renders endometrium dutiable fro implantation, inhibits FSH and LH
Oestrogen - proliferation of endometrium, inhibits FSH

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27
Q

Metabolism of NA

A

Re-uptake transporter transports it back into pre-synaptic vesicle where it is metabolised to amines by MAO

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28
Q

Metabolism of ACh

A

By acetylcholinesterase in the synapse

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29
Q

What effects rate of distribution?

A

Membrane permeability and blood perfusion

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30
Q

What effects extent of distribution?

A

Lipid solubility, pH-Pka, tissue binding, PPB

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31
Q

Competitive orthosteric antagonist?

A

Binds reversibly to the active site (same site as drug)

Prevents agonist action but can be overcome with increased agonist concentration

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32
Q

Concentration response curve of competitive orthosteric antagonist?

A

Parallel but shifted to the right

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33
Q

What does a partial agonist appear like?

A

Maximum response falls short to the maximal response a system is capable of

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34
Q

What is aciclovir best against?

A

Herpes simplex virus

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35
Q

How is aciclovir selective?

A

Needs to be phosphorylated to be effective, so utilise simplex specific kinase for monophsophorylation

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36
Q

Why can metronidazole not be taken with alcohol?

A

Metronidazole inhibits aldehyde dehydrogenase which is an enzyme needs for ethanol metabolism
Nausea, stomach pain, hot flush, palpitations

37
Q

Components on combined pill and functions?

A

Contains oestrogen and progesterone
Oestrogen inhibits FSH release via negative feedback = prevents development of follicle
Progesterone inhibits release of LH, makes cervical mucus less suitable for sperm and prevents ovulation

38
Q

What is the phase I reaction?

Aim?

A

Most commonly an oxidation reaction mediated by cytochrome P450
Addition of functional group to decrease lipid solubility
May activate pro-drugs

39
Q

Parasympathetic receptors

A
  1. Ach (neuronal nicotinic)

2. Ach (Muscarinic)

40
Q

Sympathetic receptors

A
  1. Ach (neuronal nicotinic)

2. NA (adrenoreceptor)

41
Q

What is the result of blocking K+ channels on the release of insulin?

A

Glucose into cell
Glucose –> ATP
ATP opens K+ channels and move out
When ATP high, K+ channel blocked = depolarisation = Ca2+ channel opens, Ca2+ and causes insulin release

42
Q

Depolarising block?

What molecules cause this?

A

Stimulation of muscle type nicotinic receptors by Ach cause depolarisation and contraction of muscle fibre
Muscle type nicotinic receptor agonist are not metabolised quickly by acetylcholinesterase = persistent depolarisation = loss of further excitability = depolarising block = paralysis/muscle relaxation

43
Q

What drug stimulates release of insulin?

A

Potassium channel blocker e.g. sulphonylureas

This will open Ca2+ channels and release insulin by exocytosis

44
Q

What type of reaction changes the ketone group to hydroxyl group on warfarin?

A

Phase I metabolism by cytochrome P450

45
Q

What mechanism moves drugs from blood to tissue?

A

Distribution

46
Q

What do polyenes such as nystatin and amphotericin target?

A

Bind directly to sterols in the membrane (higher affinity for ergosterol) and from ion channels in the membrane

47
Q

What type of data would be used to generate a graded response curve?

A

% response of a single person at different concentrations of drug

48
Q

What type of data would be used to generate a quantal response curve?

A

A specified response to a drug within a concentration (e.g. muscle contraction/100000) against different concentrations of a drug

49
Q

What class of drugs are highly protein bound but poorly absorbed?

A

Benzodiazepines = highly lipophilic

50
Q

Calculate volume of distribution?

A

Dose administered/concentration in blood

51
Q

If a drug has high Vd where is it likely to be found?

A

Outside of plasma, bound to tissue

52
Q

If a drug is too large to cross plasma membrane like warfarin, what will its Vd be like?

A

Low - it is confined to the plasma

53
Q

Which type of drug would have a higher Vd

a) Drugs distributed in the extracellular compartments, they cannot enter cells easily (low lipid solubility)
b) Drugs distributed in the body water, lipid soluble so can readily cross membranes?

A

b

54
Q

What hormones does the combined pill have an effect on?

A

Contains progesterone and oestrogen which provide negative feedback loops to hypothalamus and anterior pituitary to prevent GRH, LH and FSH release

55
Q

What enzyme converted paracetamol in phase I reaction?

A

CYP450 to a toxic metabolite which is detoxified by glutathione (phase II)

56
Q

In overdose how does paracetamol metabolism differ to therapeutic dose?

A

Normally metabolised mainly by phase II (glucuronic acid), and a little by phase I to a toxic metabolite which is detoxified by glutathione (phase II)
In overdoes the phase II pathways are saturated so more is metabolised by CYP450 to a toxic metabolite
Glutathione is depleted so is not detoxified = tissue damage and hepatic necrosis

57
Q

Action of cortisol?

A

Increase and maintain normal blood glucose levels by
increasing gluconeogenesis
decreasing glucose uptake into muscles and adipose
decrease in protein synthesis so AA are free fro gluconeogenesis

58
Q

Disorder of cortisol?
Cause?
Treatment?

A

Cushings syndrome = hypercortisoleamia
Adrenal or pituitary tumour or chronic glucocorticoid therapy (bushings-like symptoms not actually cushings syndrome)
Removal of tumour or use of drug that inhibits cortisol production

59
Q

Consequences of Cushing’s syndorme?

A

Buffalo hump
Hypertenison
Thin arms and legs, increased abdominal fat
Poor wound healing

60
Q

How does IV looks different to other methods of administration on graph?

A

Iv will have highest blood concentration straight away, others will start lower and gradually increase as absorption occurs

61
Q

Which combinations of the following drug classes might be used to treat inflammation?

  1. Histamine H1 antagonists
  2. Histamine H2 antagonists
  3. Glucocorticoid antagonists
  4. Glucocorticoid agonists
  5. Cyclooxygenase inducers
  6. Cyclooxygenase inhibitors
A) 2, 3 and 4
B) 1 and 2
C) 1, 3 and 5
D) 1, 4 and 6
E) 2 and 6
A

D
Histamine is an inflammatory mediator - needs to be inhibited.Different histamine receptors have different effects, H1 = inflammatory, H2 = acid secretion in the gut = not needed
Glucocorticoids are anti-inflammatory so should be stimulated
COXII = activated in inflammation = inhibited in anti-inflammation

62
Q

Mrs Beecham was given the antifungal agent, Nystatin for an oral candidiasis infection. 2 days after prescribing the treatment she returns to the clinic with low renal function. What is the likely underlying mechanism for this adverse effect?
A) Altered amino acid transport
B) Binding to 14-α demethylase
C) Hypokalaemia induced by increased cell permeability
D) Inhibition of CYP P450 function
E) Increased CYP P450 function

A

Nyastin = polyene = causes ion channels in the membrane due to binding of ergosterol = side effects to do with membrane permeability

63
Q

Describe what is meant by the term distributional selectivity?

Why is this concept important in the chemotherapy of infectious diseases?

A

More of the drug in the infected cell than the host cell (selectively accumulates into the infected cell over the host cell)
It only goes to one part of the body (administered into the infected area only)

By ensuring a higher concentration is in the infected cell than the host cell means it is non-toxic to the host cell
Chemotherapy exploits the difference between invading and host species

64
Q

What type of drug is preferably absorbed from oral (SI) route?

A

Weak bases

65
Q

Why is SI a good place for absorption?

A

Large, highly permeable, vascularised SA

Enterocytes contain drug metabolising enzymes

66
Q

Factors effecting rate of GI absorption

A

Rate of gastric emptying
Gut pH = poor absorption of strong acids and bases
Particle size
Physico-chemical interactions e.g. tetracycline binds to Ca2+ rich food

67
Q

Bioavailability

How is it calculated?

A

Fraction of administered dose entering systemic circulation

Area under the curve of a concentration time curve

68
Q

Where does 1st pass metabolism occur?

A

Liver and intestine

69
Q

pKa

A

Strength of acid/base

70
Q

pKa=pH

A

50% ionised

71
Q

Exposure to what can effect elimination?

A

Exposure to inducers or inhibitors

Increase or decrease metabolism

72
Q

3 steps of renal excretion?

A

Glomerular filtration, tubular secretion, tubular reabsorption

73
Q

Glomerular filtration dependent on:

A

Concentration of free drug in the plasma

Molecular weight

74
Q

2 systems for tubular secretion?
Effect of PPB
Competetion

A

Acid and basic
No effect from PPB because it is carrier mediated transport
Some drugs use same transporter = competition

75
Q

Tubular reabsorption dependent on:

A 
Lipid solubility (high = excreted from tubule, low = concentrate in urine)
pH of tubule fluid (alkaline = acids ionised so concentrate in urine, bases move out)
76
Q

How are NSAIDs anti-inflammatory?

A

Decreased prostaglandin cause less sensitisation fo nociceptors to effects of mediators

77
Q

Side effects of aspirin?

Why can it not be given to children?

A

GI irritation, hypersensitivity, vertigo (high dose)

In children can cause Reye’s syndrome

78
Q

Why is ibuprofen preferred over aspirin?

A

Uncommon and mild side effects, some sensitivity reactions, less GI irritation.
Suitable for children

79
Q

What effects does inflammation have on paracetamol?

A

Less analgesic effects

80
Q

Action of opioids?

A

Agonists of Mu opioid receptor which is a Gi coupled receptor

81
Q

Therapeutic effect of opioids

A

Analgesia, euphoria, sedation

82
Q

Why is administered dose of opioids higher than therapeutic dose?

A

Extensive first pass metabolism

83
Q

Opioid absorption from the gut?

A

Erratic

84
Q

Adverse effects of opioids?

A 
CNS = respiratory depression, drowsiness, sedation
PNS = constipation, histamine release, pinhole pupils
85
Q

Classification of ADR’s with examples

A 
A = Augmented = link to pharmacological action of drug e.g. bradycardia from B blockers, tachycardia from muscarinic antagonists
B = Bizarre = don't link to pharmacological action of drug e.g. anaphylaxis from penicillin
C = Chronic = as a result of chronic treatment e.g. Cushing's syndrome from glucocorticoid therapy 
D = Delayed = in patient after treatment or in children of patient after birth e.g drug in pregnant mothers found to increase risk of vaginal cancer in offspring in their 20s
E = End of treatment = withdrawal symptoms e.g. adrenal insufficiency after glucocorticoid treatment
86
Q

Fastest type of receptor?

A

Ligand gated

87
Q

Drugs that potentiate function of anti-coagulants?

A

Anti-platelet drugs e.g. Aspirin
Cytochrome P450 inhibitors
Inhibitors of Vit K reduction

88
Q

Drugs that decrease function of anti-coagulants?

A

Cytochrome P450 inducers

Drugs that reduce absorption

89
Q

Action of B1 and B2 agonists?

A

Increase HR

Bronchodilation

Stage 2 Cheat sheets (9 decks)

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